Propagation and attenuation of mechanical signals in ultrasoft 2D solids.

The propagation of elastic waves in soft materials plays a crucial role in the spatiotemporal transmission of mechanical signals, e.g., in biological mechanotransduction or in the failure of marginal solids.

Strand Plasticity Governs Fatigue in Colloidal Gels.

The repeated loading of a solid leads to microstructural damage that ultimately results in catastrophic material failure. While posing a major threat to the stability of virtually all materials, the microscopic origins of fatigue, especially for soft solids, remain elusive. Here we explore fatigue in colloidal gels as prototypical inhomogeneous soft solids by combining experiments and computer simulations.

Temperature-Triggered Colloidal Gelation through Well-Defined Grafted Polymeric Surfaces.

Sufficiently strong interparticle attractions can lead to aggregation of a colloidal suspension and, at high enough volume fractions, form a mechanically rigid percolating network known as a colloidal gel. We synthesize a model thermo-responsive colloidal system for systematically studying the effect of surface properties, grafting density and chain length, on the particle dynamics within colloidal gels. After inducing an attraction between particles by heating, aggregates undergo thermal fluctuation which we observe and analyze microscopically; the magnitude of the variance in bond angle is larger for lower grafting densities.

Linking Particle Dynamics to Local Connectivity in Colloidal Gels.

Colloidal gels are a prototypical example of a heterogeneous network solid whose complex properties are governed by thermally activated dynamics. In this Letter we experimentally establish the connection between the intermittent dynamics of individual particles and their local connectivity. We interpret our experiments with a model that describes single-particle dynamics based on highly cooperative thermal debonding.

Criticality and mechanical enhancement in composite fiber networks.

Many biological materials consist of sparse networks of disordered fibers, embedded in a soft elastic matrix. The interplay between rigid and soft elements in such composite networks leads to mechanical properties that can go far beyond the sum of those of the constituents. Here we present lattice-based simulations to unravel the microscopic origins of this mechanical synergy.

Each of the four intracellular cysteines of CD36 is essential for insulin- or AMP-activated protein kinase-induced CD36 translocation.

Stimulation of cellular fatty acid uptake by induction of insulin signalling or AMP-kinase (AMPK) activation is due to translocation of the fatty acid-transporter CD36 from intracellular stores to the plasma membrane (PM). For investigating the role of the four Cys-residues within CD36's cytoplasmic tails in CD36 translocation, we constructed CHO-cells expressing CD36 mutants in which all four, two, or one of the intracellular Cys were replaced by Ser. Intracellular and PM localization of all mutants was similar to wild-type CD36 (CD36wt).

Effects of AMPK activators on the sub-cellular distribution of fatty acid transporters CD36 and FABPpm.

In heart and skeletal muscle, enhanced contractile activity induces an increase in the uptake of glucose and long-chain fatty acids (LCFA) via an AMP-activated protein kinase (AMPK)-regulated mechanism. AMPK activation induces glucose uptake through translocation of glucose transporter 4 (GLUT4) from intracellular pools to the plasma membrane (PM). AMPK-mediated LCFA uptake has been suggested to be regulated by a similar translocation of the LCFA transporters CD36 and plasma membrane-associated fatty acid binding protein (FABPpm).

Delipidation of insect lipoprotein, lipophorin, affects its binding to the lipophorin receptor, LpR: implications for the role of LpR-mediated endocytosis.

The insect lipophorin receptor (LpR), an LDL receptor (LDLR) homologue that is expressed during restricted periods of insect development, binds and endocytoses high-density lipophorin (HDLp). However, in contrast to LDL, HDLp is not lysosomally degraded, but recycled in a transferrin-like manner, leaving a function of receptor-mediated uptake of HDLp to be uncovered. Since a hallmark of circulatory HDLp is its ability to function as a reusable shuttle that selectively loads and unloads lipids at target tissues without being endocytosed or degraded, circulatory HDLp can exist in several forms with respect to lipid loading.

Insulin-induced translocation of CD36 to the plasma membrane is reversible and shows similarity to that of GLUT4.

In cardiac and skeletal muscles, insulin regulates the uptake of long-chain fatty acid (LCFA) via the putative LCFA transporter CD36. Biochemical studies propose an insulin-induced translocation of CD36 from intracellular pools to the plasma membrane (PM), similar to glucose transporter 4 (GLUT4) translocation. To characterize insulin-induced CD36 translocation in intact cells, Chinese hamster ovary (CHO) cells stably expressing CD36 or myc-tagged GLUT4 (GLUT4myc) were created.